Cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells target infected or transformed cells with perforin-containing cytotoxic granules through immune synapses, while platelets secrete several types of granules which contents are essential for thrombosis and hemostasis. Recent work has culminated in the notion that an exocytic SNARE complex, based on a very similar set of components, is primarily responsible for exocytosis of the diverse granules in these different cell types. Granule exocytosis is, in particular, uniquely dependent on the atypical Q-SNARE syntaxin 11, its interacting partners of the Sec/Munc (SM) family, and is regulated by Rab27a. Mutations in these exocytic components underlie disease manifestations of familial hemophagocytic lymphohistiocytosis (FHL) subtypes, characterized by hyperactivation of the immune system, as well as platelet granule secretion defects. Here we discuss the key discoveries that led to the converging notion of the syntaxin 11-based exocytosis machinery for cytotoxic granules and platelet-derived granules.

细胞毒性T淋巴细胞（CTL）和自然杀伤（NK）细胞通过免疫突触以含有穿孔素的细胞毒性颗粒靶向感染或转化的细胞，而血小板分泌几种类型的颗粒，其含量对于血栓形成和止血至关重要。最近的工作最终形成了这样的观点，即基于非常相似的一组组分的胞外SNARE复合体主要负责这些不同细胞类型中各种颗粒的胞吐作用。颗粒胞吐特别是特别依赖于非典型Q-SNARE语法11，它是Sec / Munc（SM）家族的相互作用伴侣，并受Rab27a调控。这些胞外成分的突变是家族性噬血细胞淋巴组织细胞增生症（FHL）亚型的疾病表现的基础，其特征是免疫系统过度活化，以及血小板颗粒的分泌缺陷。在这里，我们讨论了关键发现，这些发现导致基于语法11的胞吐机制对细胞毒性颗粒和血小板衍生颗粒的融合。